Abstract | BACKGROUND: OBJECTIVE: To analyze the role of MUC1 in corticosteroid effectiveness in different cohorts of patients with CRSwNP and elucidate the possible mechanisms involved. METHODS: Seventy-three patients with CRSwNP took oral corticosteroids for 15 days. Corticosteroid resistance was evaluated by nasal endoscopy. The expression of MUC1 and MUC1 CT was evaluated by real-time PCR, Western blotting, and immunohistochemistry. Beas-2B knockdown with RNA interference for MUC1 (siRNA-MUC1) was used to analyze the role of MUC1 in the anti-inflammatory effects of dexamethasone. RESULTS: CONCLUSION: MUC1-CT participates in the corticosteroid response that mediates GRα nuclear translocation. The low expression of MUC1 in patients with CRSwNP may participate in corticosteroid resistance.
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Authors | Javier Milara, Teresa Peiró, Miquel Armengot, Soledad Frias, Anselm Morell, Adela Serrano, Julio Cortijo |
Journal | The Journal of allergy and clinical immunology
(J Allergy Clin Immunol)
Vol. 135
Issue 2
Pg. 470-6
(Feb 2015)
ISSN: 1097-6825 [Electronic] United States |
PMID | 25159466
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2014 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved. |
Chemical References |
- Adrenal Cortex Hormones
- Anti-Inflammatory Agents
- Mucin-1
- Receptors, Glucocorticoid
- Toll-Like Receptors
- glucocorticoid receptor alpha
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Topics |
- Adrenal Cortex Hormones
(therapeutic use)
- Anti-Inflammatory Agents
(therapeutic use)
- Chronic Disease
- Down-Regulation
- Drug Resistance
(genetics)
- Gene Expression Regulation
- Humans
- Mucin-1
(genetics)
- Nasal Mucosa
(drug effects, metabolism)
- Nasal Polyps
(complications)
- Receptors, Glucocorticoid
(genetics, metabolism)
- Rhinitis
(complications, drug therapy, genetics, metabolism)
- Signal Transduction
- Sinusitis
(complications, drug therapy, genetics, metabolism)
- Toll-Like Receptors
(genetics)
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